Propofol Protects Against Hepatic Ischemia Reperfusion Injury via Inhibiting Bnip3-Mediated Oxidative Stress

Ma, Hongyan; Liu, Ying; Li, Zhengtian; Yu, Li; Gao, Yang; Ye, Xiangmei; Yang, Baoyi; Li, Hulun; Shi, Jinghui

doi:10.1007/s10753-021-01416-z

Cited by 11 publications

(9 citation statements)

References 28 publications

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“…We examined the effects of propofol-induced oxidative stress injuries on reactive oxygen species (ROS) and ATP levels, and apoptosis in hippocampal neurons. Previous studies (34,35) have shown that propofol could increase mitochondrial ROS levels, decrease ATP levels, and increase mitochondrial-mediated activation of Apaf-1, cleaved caspase-9, and CytC apoptotic factors in hippocampal neurons, ultimately leading to hippocampal neuronal apoptosis. Respiratory chain inhibitors can have similar effects, which suggests that propofol might act on the mitochondrial respiratory chain (36).…”

Section: Discussionmentioning

confidence: 95%

Propofol produces neurotoxicity by inducing mitochondrial apoptosis

et al. 2022

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Propofol is a fast and short-acting intravenous anesthetic widely used in clinical anesthesia and intensive care unit sedation. However, its use can cause abnormal effects on the central nervous system. Thus, the purpose of this study was to investigate the mechanism of propofol on primary hippocampal neuron injury. In addition, we aimed to determine whether a correlation exists between propofol and mitochondrial apoptosis-induced neurotoxicity. Hippocampal neurons cultured for 4 days were exposed to different drugs. The treatment groups were divided according to drug exposure into propofol, a rotenone inhibitor, and a coenzyme Q10 agonist groups. The final concentrations of propofol were 1, 10 and 100 µM. The content of ATP and reactive oxygen species (ROS) in the neurons of each group were detected using commercial kits in the culture supernatant after 3 h of drug exposure. Western blotting was used to analyze the expression of apoptosis-related proteins. The JC-1 kit was used to detect the mitochondrial membrane potential. The results revealed that, compared with the non-propofol treatment groups, the expression of apoptosis-related proteins, ATP content, and mitochondrial membrane potential were significantly decreased while the ROS content was markedly increased in the propofol treatment group. In conclusion, propofol treatment promoted damage to hippocampal neuronal mitochondria in a dose-dependent manner. This damage may lead to neuronal apoptosis and neurotoxicity by inducing the inhibition of mitochondrial respiratory chain complex I.

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Section: Discussionmentioning

confidence: 95%

Propofol produces neurotoxicity by inducing mitochondrial apoptosis

et al. 2022

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“…Recent studies have confirmed that oxidative stress plays a key role in liver I/R injury. , Meanwhile, we found that CNDs possess the ability of ROS to scavenge in our previous study. , Therefore, we further explored whether the suppression of oxidative stress during HIRI accounts for the protective effect of CNDs against HIRI. Subsequently, we performed DHE staining to detect ROS levels and in Figure A, intracellular ROS concentrations in CNDs-treated mice were obviously decreased in comparison with those in the NSS group subjected to hepatic I/R insult.…”

Section: Resultsmentioning

confidence: 81%

“…Recent studies have confirmed that oxidative stress plays a key role in liver I/R injury. 25,26 Meanwhile, we found that CNDs possess the ability of ROS to scavenge in our previous study. 16,17 Therefore, we further explored whether the suppression of oxidative stress during HIRI accounts for the protective effect of CNDs against HIRI.…”

Section: Cnds Inhibit Liver Oxidative Stress Injury Duringmentioning

confidence: 87%

Nitrogen-Doped Carbon Dots with Oxidation Stress Protective Effects for Reactive Oxygen Species Scavenging on Hepatic Ischemia–Reperfusion Injury

Chen

Wang

et al. 2023

ACS Appl. Nano Mater.

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Hepatic ischemia−reperfusion injury (HIRI), which is a common pathophysiological process that occurs in hepatectomy, affects the survival and prognosis of patients. In this study, we synthesized chitosan-derived nitrogen-doped carbon dots (CNDs) with reactive oxygen species (ROS) scavenging capabilities and applied them in the prevention of HIRI. CNDs demonstrated scavenging ability against ROS, particularly hydroxyl radicals. Our results show that CNDs can alleviate liver damage in mice, suppress the inflammatory response, and inhibit apoptosis triggered by liver ischemia/reperfusion (I/R) operation. Mechanistically, CNDs exhibit hepatoprotective effects on I/R injury due to the clearance of ROS. In summary, CNDs protect the liver against ischemia−reperfusion injury by suppressing oxidative stress damage.

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“…28 TNF-α is mainly produced by Kupffer cells, and it is not only involved in inflammatory reaction, but also related to liver regeneration. 29 IL-10 can down regulate TNF-α during HIRI. 30 In the presented study, overexpression of miR-146a remarkably inhibited the increased levels of TNF-α, IL-6, but increased the concentration of IL-10 after HIRI induction (Figure 4D).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-146a Improved Acute Lung Injury Induced by hepatic Ischemia-reperfusion Injury by Inhibiting PRDX1

Chen

Yao

et al. 2023

Dose-Response

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Hepatic ischemia-reperfusion injury (HIRI)–induced acute lung injury (ALI) is characterized by high incidence and poor prognosis. The regulatory role of microRNA-146a (miR-146a) in HIRI has been reported, but if miR-146a could affect the progression of HIRI-induced ALI has not been reported. The mice HIRI model was established by ligating left hepatic portal vein and hepatic artery for 60 minutes and then treating with reperfusion for 4 hours. Hypoxia-reoxygenation (HR) was performed to establish cell model. The binding site between miR-146a and Peroxidase 1 (PRDX1) was predicted and validated. The levels of inflammation factors and redox markers were detected with commercial kits. Significant lower expression of miR-146a and higher expression of PRDX1 in HIRI animal model were observed. miR-146a inhibited the liver injury after HIRI induction through targeting PRDX1. miR-146a inhibited the lung injury caused by HIRI via regulating PRDX1. The inhibition of cell apoptosis and inflammation factors by miR-146a were reversed by pcDNA-PRDX1. This research demonstrated that miR-146a improved ALI caused by HIRI by inhibiting apoptosis, inflammation, oxidative condition through targeting PRDX1. This study might provide a novel thought for the prevention and treatment of ALI caused by HIRI by regulating miR-146a/PRDX1 axis.

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Propofol Protects Against Hepatic Ischemia Reperfusion Injury via Inhibiting Bnip3-Mediated Oxidative Stress

Cited by 11 publications

References 28 publications

Propofol produces neurotoxicity by inducing mitochondrial apoptosis

Propofol produces neurotoxicity by inducing mitochondrial apoptosis

Nitrogen-Doped Carbon Dots with Oxidation Stress Protective Effects for Reactive Oxygen Species Scavenging on Hepatic Ischemia–Reperfusion Injury

MicroRNA-146a Improved Acute Lung Injury Induced by hepatic Ischemia-reperfusion Injury by Inhibiting PRDX1

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